SYVN1 (Synoviolin 1)

The functional interplay between LOXL2 and SYVN1 drives LIHC progression through the ECM-ERS-ERAD regulatory axis, and dual targeting of this axis may represent a potential therapeutic strategy.

Furthermore, our findings clarified that DDX5 and eEF1A2 mediated the stimulative function of SYVN1 in ESCC progression and NF-κB pathway was responsible for the effects of SYVN1/DDX5/eEF1A2 axis on ESCC. Overall, this study illustrated that SYVN1 promoted the M2 polarization of TAMs to induce ESCC progression by targeting DDX5 and eEF1A2 to activate NF-κB pathway.

Significantly, LS-102 in combination with the EGFR-TKI AZD9291 exhibits strong inhibitory effects on NSCLC growth and reverses the resistance of NSCLC to AZD9291. Together, our study demonstrates that the SYVN1-EGFR axis plays a critical role in NSCLC development and suggests that targeting the SYVN1-EGFR axis to destabilize EGFR may represent a putative therapeutic strategy for TKI-resistant NSCLC.

Thus, SYVN1 may inhibit the proliferation, migration, and invasion of PTC cells by disrupting HMGB1. Consequently, SYVN1 might be considered a promising therapeutic target for PTC.

Biologically, SYVN1 knockdown successfully compromises cell proliferation and tumour xenograft growth in mouse models that can be partially rescued by overexpression of MCT4. Clinicopathologically, overexpression of SYVN1 is associated with poor prognosis in patients with LUAD, highlighting the importance of the SYVN1-MCT4 axis, which performs metabolic reprogramming during the progression of LUAD.